Studies on the role of 'start' lipid trafficking proteins in macrophage lipid homeostasis

• Main Author: Borthwick, Faye
• Published: Glasgow Caledonian University 2009
• Subjects: 616.3997
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496152

Steroidogenic acute regulatory (StAR) related-lipid transfer (START) proteins (STARD1-STARD15) are suggested to play a role in cholesterol homeostasis and atherosclerosis, and are potential drug targets by virtue of their lipid binding domains. Members of the STARD1 subfamily (STARD1, STARD3) of lipid trafficking 'START' proteins can reduce macrophage lipid content and inflammatory status (STARD1; StAR), and traffic cholesterol from the endosomes (STARD3/MLN64) All of the 'START' family members were found to be expressed in human heart aorta, peripheral blood monocytes and human THP-1 monocytes, except testis-specific STARD6. Phorbol ester-Induced differentiation of THP-1 monocytes to macrophages (7 days) induced two-fold or greater Increases in gene expression of STARD4, STARDd, STARD9 and STARD14, whereas levels of STARD3 mRNA declined. Treatment with acetylated LDL increased gene expression of STARD4, STARD10, STARD12 more than two-fold, but levels of STARDl STARD2, STARD7, STARDd, STARD9 and STARD14 mRNA declined significantly.